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(− 7402 T/G and-4729G/A) condition susceptibility to pediatric severe malarial anemia but not circulating IL-13 levels

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dc.contributor.author Okumu, Wilson
dc.contributor.author Okeyo, Winnie A
dc.contributor.author Munde, Elly O
dc.contributor.author Raballah, Evans
dc.contributor.author Anyona, Samuel B
dc.contributor.author Vulule, John M
dc.contributor.author Ong’echa, John M
dc.contributor.author Perkins, Douglas J
dc.contributor.author Ouma, Collins
dc.date.accessioned 2018-06-28T06:53:58Z
dc.date.available 2018-06-28T06:53:58Z
dc.date.issued 2013
dc.identifier.uri https://repository.maseno.ac.ke/handle/123456789/639
dc.description.abstract In holoendemic Plasmodium falciparum transmission areas such as western Kenya, severe malarial anemia [SMA, hemoglobin (Hb) < 6.0 g/dL, with any density parasitemia] is the most common clinical manifestation of severe malaria resulting in high rates of pediatric morbidity and mortality in these regions. Previous studies associated interleukin (IL)-13 with pathogenesis of different infectious diseases, including P. falciparum malaria. However, the functional roles of polymorphic variants within the IL-13 promoter in conditioning susceptibility to SMA remain largely unexplored. As such, the association between the IL-13 variants -7402 T/G (rs7719175) and -4729G/A (rs3091307) and susceptibility to SMA was determined in children (n = 387) presenting with clinical symptoms of falciparum malaria and resident in a holoendemic transmission region in western Kenya. Our results indicated no difference in the proportions of individual genotypes among children presenting with non-SMA (n = 222) versus SMA (n = 165). Similarly, there was no associations between the individual genotypes (−7402 T/G and -4729G/A) and SMA. Additional analyses, however, revealed that proportions of individuals with -7402 T/-4729A (TA) haplotype was significantly higher in children presenting with SMA than non-SMA group (P = 0.043). A further multivariate logistic regression analyses, controlling for confounding factors, demonstrated that carriage of the TA haplotype was associated with increased susceptibility to SMA (OR; 1.564, 95% CI; 1.023-2.389, P = 0.039). In addition, circulating levels of IL-13 were comparable between the clinical groups as well as across genotypes and haplotypes. Collectively, findings presented here suggest that haplotypes within the IL-13 promoter at -7402 T/G and -4729G/A may modulate SMA pathogenesis, but do not affect circulating IL-13 levels en_US
dc.publisher Bio Med Central en_US
dc.subject : IL-13, Promoter polymorphisms, Haplotypes, Severe malaria anemia en_US
dc.title (− 7402 T/G and-4729G/A) condition susceptibility to pediatric severe malarial anemia but not circulating IL-13 levels en_US
dc.type Article en_US


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